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Regular Article |
a Center for Reproductive Medicine, Departments of Physiology and of Obstetrics and Gynecology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden
b Institute of Anatomy and Cell Biology, Medical Faculty, Göteborg University, SE-405 30 Göteborg, Sweden
ABSTRACT
Almost all ovarian follicles undergo atresia during follicular development. However, the number of corpora lutea roughly equals the number of preovulatory follicles in the ovary. Because apoptosis is the cellular mechanism behind follicle and luteal cell demise, this suggests a change in apoptosis susceptibility during the periovulatory period. Sex steroids are important regulators of follicular cell survival and apoptosis. The aim of the present work was to study the role of progesterone receptor-mediated effects in the regulation of granulosa cell apoptosis. The levels of internucleosomal DNA fragmentation were evaluated in rat granulosa cells before and after induction of the nuclear progesterone receptor, using hCG treatment to eCG-primed rats to mimic the naturally occurring LH surge. Granulosa cells isolated from hCG-treated rats showed a several-fold increase in the expression of progesterone receptor mRNA and a 47% decrease (P < 0.01) in DNA fragmentation after 24 h incubation in serum-free medium compared to granulosa cells isolated from rats treated with eCG only. The effect of hCG treatment in vivo was dose-dependently reversed in vitro by addition of antiprogestins (Org 31710 or RU 486) to the culture medium, demonstrated by increased DNA fragmentation as well as increased caspase-3 activity. Addition of antiprogestins to granulosa cells isolated from immature or eCG-treated rats did not result in increased DNA fragmentation. The results suggest that progesterone receptor-mediated effects are involved in regulating the susceptibility to apoptosis in LH receptor-stimulated preovulatory rat granulosa cells.
First decision: 10 March 2000.
1 This work was supported by grants 10380 and 11134 from The Swedish MRC, by grants from the Assar Gabrielsson Foundation, The Research Foundation of Hjalmar Svensson, The Göteborg Medical Society, The Foundation of Clas Groschinskys Memorial Fund, and by grants from the State under the LUA agreement.
2 Correspondence: Håkan Billig, Department of Physiology, P.O. Box 434, SE-405 30, Göteborg, Sweden. FAX: 46 31 7733531; hakan.billig{at}fysiologi.gu.se
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